Notch signalling: a simple pathway becomes complex
By S. Bray. Nature reviews. Molecular cell biology, 2006
2,725 citations recorded by the source corpus.
Subfields: Molecular Biology
View Paper: https://www.semanticscholar.org/paper/b4e120667bcf0cc243110770d012a2105672ba61
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Citations in the corpus
- Hippo signaling in organ size control. (2007, background): “Hpo signaling in other developmental processes A recurring theme in developmental biology is the use of a single signaling cascade in multiple, and sometimes seemingly unrelated, biological processes (e.g., see Bray 2006).”
- Notch signaling: the core pathway and its posttranslational regulation. (2009, background): “…highly regulated and the net result is intramembrane proteolysis of the intact, membrane-bound Notch receptor and consequent release of a soluble fragment consisting of the entire intracellular domain, termed Notch intracellular domain (NICD; Figure 1; reviewed in Bray, 2006; Gordon et al., 2008).”
- The notch ligands Dll4 and Jagged1 have opposing effects on angiogenesis. (2009, neutral): “However, the regulation of endothelial cell (EC) sprouting and proliferation also involves intrinsic signaling interactions between ECs that are, for example, mediated by the Notch pathway (Bray, 2006; Roca and Adams, 2007).”
- The mammalian ovary from genesis to revelation. (2009, background): “The NICD translocates to the nucleus and interacts with the DNA-binding CSL [CBF1, Su(H), and Lag-1] transcription factor and its coactivator, Mastermind, to promote transcription (147).”
- iNOS promotes CD24+CD133+ liver cancer stem cell phenotype through a TACE/ADAM17-dependent Notch signaling pathway (2018, background): “Notch signaling promotes the progression of solid cancers (22) by driving angiogenesis (23) and maintaining a population of undifferentiated CSCs. Notch signaling is triggered when the Notch receptor is cleaved/activated at site 2 (S2; Val1711) (24) by ADAM (a disintegrin and metalloprotease) 10 or ”
- The Canonical Notch Signaling Pathway: Unfolding the Activation Mechanism (2009, background): “…although the CSL protein RBPjκ can form complexes with many ubiquitous corepressor proteins, such as CIR, FLH1C/KyoT2, and NCoR/SMRT (reviewed in Bray, 2006), it is SHARP/MINT/SPEN that has emerged as the critical repressor of Notch target genes in vivo (Oswald et al., 2005; Tsuji et al.,…”
- Notch–RBP-J signaling controls the homeostasis of CD8− dendritic cells in the spleen (2007, background): “The Notch signaling pathway is an evolutionarily conserved mechanism regulating the development of multiple cells and tissues (13).”
- Engineering T cells with Customized Therapeutic Response Programs Using Synthetic Notch Receptors (2016, neutral): “When it engages the cognate antigen, the synNotch receptor undergoes induced transmembrane cleavage, akin to native Notch activation (Bray, 2006; Selkoe and Kopan, 2003), thereby releasing the intracellular transcriptional domain to enter the nucleus and activate expression of target genes regulated”
- A phase I trial of the γ-secretase inhibitor MK-0752 in combination with gemcitabine in patients with pancreatic ductal adenocarcinoma (2018, background): “The Notch pathway is involved in the development, differentiation, growth and fate of multiple different cell types (Bray, 2006), and has a fairly limited set of known target genes, including transcriptional regulators Hes (hairy/enhancer of split) and Hey (subfamily of Hes) (Borggrefe and Oswald, 2”
- Hypoxia-inducible factors in stem cells and cancer (2009, neutral): “Signalling is initiated when the Jagged or Delta family of ligands binds a Notch receptor, triggering a two-step receptor proteolysis event [59].”
- Molecular regulation of angiogenesis and lymphangiogenesis (2007, background): “This complex allows the expression of basic helix–loop–helix (bHLH) proteins of the hairy/enhancer-of-split-related transcription factor family — Hey2 and Her in zebrafish, and Hey and Hes in mammals — which, in turn, control the expression of other downstream target gene”